Congestive heart failure is a serious condition that affects the pumping ability of the heart. The condition often manifests itself within the cardiac cycle as an abnormal diastole phase (diastolic heart failure) or systole phase (systolic heart failure).
Diastolic heart failure (DHF) often involves an abnormally slow relaxation of the heart muscle during diastole, and a high peaking pressure. This peaking pressure is often referred to as afterload. The left ventricle may become stiff and non-compliant, thus inhibiting easy filling with the available filling pressure, or “preload.” Consequently, in order to achieve a given volume, more pressure is needed. This, in turn, causes the heart to work harder. Ultimately, diastolic heart failure leads to systolic heart failure.
Generally, systolic heart failure (SHF) involves an abnormally large resting volume. The larger volume corresponds to increased heart wall tension or strain, thinner heart walls, and other related problems that lead to tissue damage. A positive destructive feedback loop often develops, resulting eventually in total cardiac failure.
As an aid in understanding diastolic and systolic heart failure, pressure-volume (PV) loops for the left ventricle of 1) a healthy heart, 2) a heart experiencing systolic heart failure, and 3) a heart experiencing diastolic heart failure are illustrated as superimposed graphs in FIG. 1.
During the filling portion, represented by the segments a, a′ and a″, the DHF and SHF segments exhibit an increase in pressure as the volume increases. In contrast, the normal heart pressure remains relatively constant. For the isovolumetric contraction segment b, b′ and b″, the volume stays relatively constant for all three curves while the pressure spikes as the heart contracts. As the heart ends systole and goes through the ventricular ejection segment c, c′, c″, the pressure in the normal heart remains relatively constant with decreasing volume, while significant pressure drops are exhibited by the SHF and DHF curves. During the last component of the cycle, the pressure drops to a minimal filling level as volume is minimized.
In addition to the individual curve segment differences between the normal heart, and DHF and SHF, significant overall shifts in the curves are apparent. For DHF, the curve (as shown by segments a″, b″, c″ and d″) exhibits a distinctive upward pressure shift, and a more constrained range in volume (beginning higher than normal at the start of the cycle, but maximizing at a value less than normal). The SHF curve (a′, b′, c; and d′) exhibits a more pronounced shift outward in volume and a more constrained pressure range.
Conventional methods of treating congestive heart failure typically focus on drug therapy and lifestyle changes. Pacing therapy has also been employed through the use of implantable cardiac stimulation devices. These devices, such as pacemakers, implantable cardioverter defibrillators (ICD's) or cardiac resynchronization therapy devices (CRT), typically monitor cardiac arrhythmias, and in most cases, provide a form of electrical stimulation therapy to the heart as needed. Modern electronics have enabled the miniaturization of these devices for implantation in a patient for constant monitoring.
One proposed method for optimizing the hemodynamic parameters for a heart in CHF using an implantable cardiac device monitors and adjusts the atrioventricular delay (AV delay) for the heart in an effort to optimize hemodynamics during steady state. While this approach appears beneficial for its intended purpose, it does not suggest how to reverse the detrimental remodeling caused by CHF as shown in FIG. 1.
What would be desirable is a method of shifting the P-V loop curve for a heart experiencing congestive heart failure to a more normal curve with corresponding improvements in the heart's hemodynamic parameters.